Voss K M, Herberg L, Kern H F
Cell Tissue Res. 1978 Jul 27;191(2):333-42. doi: 10.1007/BF00222428.
A study of the pancreatic islets of Langerhans in the Djungarian hamster (Phodopus sungorus) was initiated by the observation that 98 percent of the animals of a recently established colony showed ketoacidosis soon after birth, about ten percent of which later developed persistent hyperglycemia. The islets are made up of a centrally located mass of insulin-producing B-cells surrounded by a peripheral rim of A- and D-cells. Most islets are richly supplied by unmyelinated nerve fibers which terminate on all three cell types with cholinergic synaptic endings. Early changes in islet fine structure due to ketosis comprise degranulation of A-cells combined with signs of crinophagia of alpha-granules. After the manifestation of hyperglycemia, degranulation of B-cells is followed by deposition of glycogen which in the late phase of the diabetic syndrome forms large masses obscuring the regular cellular organelles. In six- to nine-month hyperglycemic animals degenerative changes are also observed in D-cells in the form of autophagic vacuoles.
对黑线毛足鼠(Phodopus sungorus)胰岛的研究始于一项观察,即一个新建立的种群中98%的动物在出生后不久就出现了酮酸中毒,其中约10%后来发展为持续性高血糖。胰岛由位于中央的一团产生胰岛素的B细胞组成,周围是A细胞和D细胞的外周边缘。大多数胰岛由无髓神经纤维丰富供应,这些神经纤维以胆碱能突触末梢终止于所有三种细胞类型。酮症导致的胰岛精细结构早期变化包括A细胞脱颗粒以及α颗粒的噬粒现象。高血糖出现后,B细胞脱颗粒,随后糖原沉积,在糖尿病综合征后期形成大量物质,使正常细胞器模糊不清。在6至9个月的高血糖动物中,D细胞也出现了自噬泡形式的退行性变化。